Atherosclerotic coronary artery disease is a leading cause of death in industrialized countries. An atherosclerotic plaque is a thickening in the wall of the artery. Typically, patients who die of coronary disease may have several atherosclerotic plaques; however, in most instances of myocardial infarction, cardiac arrest, or stroke, it is found that only one of these potential obstructions had, in fact, ruptured, fissured, or ulcerated. The rupture, fissure, or ulcer typically causes a large thrombus to form on the inside of the artery, which may completely occlude the flow of blood through the artery, thereby injuring the heart and/or the brain.
Plaque, a thickening in the arterial vessel wall results from the accumulation of cholesterol, proliferation of smooth muscle cells, secretion of a collagenous extracellular matrix by the cells, and accumulation of macrophages and eventually, hemorrhage (bleeding), thrombosis (clotting), and calcification. The consensus theory is that atherosclerotic plaque develops as a result of irritation or biochemical damage to the endothelial cells which line the inner surface of the blood vessel. Endothelial cells normally prevent inappropriate formation of blood clots and inhibit contraction and proliferation of the underlying smooth muscle cells. Most investigators believe that atherosclerotic plaques can develop when endothelial cells are damaged or dysfunctional. Dysfunctional endothelial cells typically result from cigarette smoking, high serum cholesterol (especially oxidized low density lipoprotein), hemodynamic alterations (such as those found at vessel branch points), some viruses (herpessimplex, cytomegalovirus) or bacteria (e.g., chlamydia), hypertension, some hormonal factors in the plasma, and other factors as yet unknown. As a result of these gradual injuries to the endothelial cells, an atherosclerotic plaque may grow slowly over many years.
When a plaque rupture develops, there is typically a hemorrhage into the plaque through a fissure where the surface of the plaque meets the bloodstream. A thrombus quickly forms upon contact with the collagen and lipid of the plaque. This blood clot may then grow to completely occlude the vessel, or it may remain only partly occlusive. In the latter case, the new clot quite commonly becomes incorporated into the wall of the plaque, creating a larger plaque.
The condition of plaque deposits can vary. For example, the plaque can be inflamed and unstable, or the plaque can be quite stable. Plaque deposits that are at risk of rupturing are sometimes referred to as vulnerable plaque. Vulnerable plaque typically include a core of soft material covered with a fibrous cap. Many of vulnerable plaque deposits do not limit the flow of blood through the blood vessels. It has recently been appreciated that vulnerable plaques that do not limit flow may be particularly dangerous because they produce no warning symptoms, and can suddenly rupture causing heart attack, stroke, and/or death by forming a blood clot inside the blood vessel lumen and causing a blockage, for example.